Dialogue and Diagnosis - American Osteopathic Association

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One of the reasons for this lack of metabolic control in patients with type 2 diabetes mellitus (T2DM) is a continued clinical inertia regarding treatment intensification and adjustment 5 and an underuse of insulin in T2DM patients. 6 Poor glycemic control may be reflected in the failure of self-management by patients with diabetes mellitus, and inadequate intervention strategies by clinicians. 7-11 Attaining target glucose levels under various daily conditions—while avoiding hypoglycemia, dramatic excursions in blood glucose, and weight gain— can be difficult to achieve. Physicians need to overcome clinical inertia and intensify therapy in an appropriate and timely manner. 7 Because T2DM is a progressive disease, many patients will ultimately need insulin therapy to achieve and maintain adequate glycemic control. Insulin remains essential treatment for patients with T2DM after oral therapy alone becomes inadequate. The present article offers a case report to highlight the need for intensification and adjustment of insulin therapy in patients with T2DM. It also reviews factors that can impact achievement of treatment goals, challenges in adding medications to therapeutic regimens, and special challenges related to ethnic minorities and patient education. Report of case Sam is a 46-year-old Hispanic man who presented to his primary care physician for follow-up treatment for his T2DM. He went unwillingly but came at the urging of his wife who helped him realize that disease control is important for staying healthy. His experience with diabetes has not been good. He had vivid memories from early childhood of his grand mother receiving insulin injections from his mother. His grandmother lost her vision soon after starting insulin. She could not fill the syringe by herself and required help with her therapy. As Sam aged, he remained slim and active. Nevertheless, diabetes mellitus still developed in Sam. Three years ago, when his glycosylated hemoglobin (HbA 1c ) level was found to be 7.3%, he grudgingly agreed to begin self-monitoring of his blood glucose levels and to take metformin twice daily. Much to his surprise, his glucose control improved, and his HbA 1c level was 6.3%. A year later, despite following his nutritionist’s suggestions and exercising even more, Sam’s fasting plasma glucose level (FPG) level increased, and his HbA 1c level rose to 7.7%. He initially refused additional medications, but he later agreed to use glipizide (a sulfonylurea), noting that he preferred a medication that had been “tried and true” for many years and he did not want to take injections. The addition of glipizide to Sam’s therapy worked only transiently. At the time of his follow-up to his primary care physician, he had not seen the doctor for 9 months because his FPG values had remained between 220 and 250 mg/dL and he did not want to know the next steps. He said he did not want to “take shots” and suffer as his grandmother had. His physician was empathetic. Sam’s weight was stable and his body mass index was 24. His blood pressure was 118/76 mm Hg, despite 2 Dialogue and Diagnosis // September 2012
the fact that he was obviously upset at the time it was measured. His HbA 1c level was 9.1%. As his phenotype was not typical for T2DM, and his treatment had little durability despite his significant lifestyle efforts the consideration for atypical types of diabetes was entertained. These patients may be the “thin diabetics” and often have family history of other autoimmune diseases. Nearly 10% of adults (>35 y/o) who think they have T2DM actually have a slowly progressive form of T1DM. Autoimmune antibodies (GAD65) were ordered as was the test for endogenous glucose production (c-peptide in conjunction with serum glucose). Alternatively, people from ethnic minorities, especially men of African descent can have a form of T2DM that is prone to go to diabetic ketoacidosis. This has been termed ketosis prone T2DM or “Flatbush diabetes”—named after a street in the Bronx in which this pattern was first described. Islet-cell cytoplasm autoantibodies and glutamic acid decarboxylase autoantibodies (GADAs) can occur in patients with apparently typical T2DM. Data from the United Kingdom Prospective Diabetes Study 25, or UKPDS 25 12 showed that among patients older than 45 years, the presence of GADAs was highly predictive of the likelihood of insulin requirements. In the ADOPT trial, 10% of the T2DM study population had GAD antibodies. 13 The (GAD65) antibody was negative and his c-peptide was normal despite mild hyperglycemia (FSG 140 mg/dl). Sam’s physician explained that in light of his significant hyperglycemia and the fact he has contributed so significantly to his control that insulin would be the safest and most effective therapy. The physician also explained that insulin has been a “tried and true” life-saving therapy for almost a century. Also as a hormone replacement it may have less side effects and drug interactions than most oral medications. As a side note, if Sam were not slim and if he had a preponderance of postprandial hyperglycemia without an elevated fasting blood glucose level, then the short-acting glucagon-like peptide-1 (GLP-1) receptor agonist exenatide would be a treatment option. Because the longeracting GLP-1 receptor agonists lower both fasting and postprandial blood glucose levels, they would also be options in this type of case, especially if weight loss is a consideration. However, because Sam was relatively slim with high FPG and HbA 1c levels, insulin was his best option for therapeutic addition. Sam was instructed regarding how to use an insulin pen, including the appropriate injection sites (ie, abdomen, outer arms, and thighs). See Figure 1. Upon placing the needle on the pen, he was shown how to do a 2-unit “air-shot” (ie, dialing up the pen to 2 units and ejecting a drop of insulin into the air to ensure that the injection would deliver the correct Figure 1. Site selection for insulin injection. The most common injection site is the abdomen or stomach. Other sites that can be used include the back of the upper arms, the upper buttocks or hips, and the outer side of the thighs. These sites are recommended because they have a layer of fat just below the skin to absorb the insulin but not many nerves, which means that injection at the site will be more comfortable to the patient than injection in other parts of the body. Injection at these sites also make it easier for the patient to inject into the subcutaneous tissue. amount of insulin with no air bubbles). When administering the injection, he was advised to count to 6 to ensure that the full dose of insulin was delivered prior to withdrawing the needle from the injection site. The needle for the pen was short and 32 gauge. Sam was amazed how small and thin the needles were and was pleasantly surprised that he did not feel pain with the injection. Part of the education provided to Sam was to stress that the needle should be changed with each injection. Sam began injecting 10 units of a basal insulin analog every night at bedtime. The PREDICTIVE 303 algorithm was given to Sam to enable him to self-titrate his insulin (Table 1). 14 He had always checked his fasting blood glucose levels daily and was amenable to being even more involved with his therapy, with the assurance that he would receive guidance from his physician. Increased self-monitoring of blood glucose levels gave him further feedback and a sense of empowerment. His fasting blood sugar (FBS) goal was between 80 and 130 mg/dL, which was individualized to his situation and which is a bit more lenient than Dialogue and Diagnosis // September 2012 3
Page 1 and 2: Volume 2 Number 2 September 2012 In
Page 3: Introducing and adjusting injectabl
Page 7 and 8: insulin therapy include a sense of
Page 9 and 10: Basal insulin alone Sequential addi
Page 11 and 12: speaking Hispanic patients reported
Page 13 and 14: AFTER METFORMIN Introducing and tit
Page 15 and 16: Figure 1. The simultaneously increa
Page 17 and 18: Figure 3. Key benefits and risks of
Page 19 and 20: Compounds Exenatide (approved 2005
Page 21 and 22: PATIENT DIALOGUE Are GLP-1 receptor
Page 23 and 24: missed and the next scheduled dose
Page 25 and 26: Adding glucagon-like peptide-1 rece
Page 27 and 28: hips, which, with her excess weight
Page 29 and 30: T2DM is achieving glycemic control
Page 31 and 32: Patient instruction Clearly discuss
Page 33 and 34: 8-point glucose levels) and did so
Page 35 and 36: InsideOut (continued from inside fr

Dialogue and Diagnosis - American Osteopathic Association

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